期刊
CORONARY ARTERY DISEASE
卷 11, 期 1, 页码 41-46出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00019501-200002000-00008
关键词
atherosclerosis; infectious aetiology; AIDS; coronary artery disease in young people
Objective To determine the type of lesions observed in young patients infected with human immunodeficiency virus-1 (HIV-1), Design Examination of coronary networks in corpses of 13 men and two women who had died aged 23-32 years after having been infected with HIV-1 virus, having been seropositive for 2-5 years. Causes of death were infectious complications (five cases), infection with cytomegalovirus leading to gastrointestinal haemorrhaging (one case), infection with cytomegalovirus and Kaposi's sarcoma (one case), overdoses of drugs (five cases) and sudden death (three cases). Methods The pathological analysis was carried out on the proximal and distal coronary networks, In order to characterize the lesions better, the cells and the cytokines involved were characterized by immunohistochemistry. Results In all 15 cases we observed thickening of intima in the proximal network at least as great as that of the media, caused by a proliferation of secreting cells, phenotypically identified as smooth muscle cells, with exaggerated production of elastic fibres and in association with an increase in the expression of tumor necrosis factor-alpha and interleukin-1 alpha. In nine cases, atherosclerosis had developed from and on the surface of this proliferation and in four cases arteriosclerosis had an unusual appearance, in the form of mamillated vegetations with endoluminal protrusions. A similar proliferation was found in the distal network in four cases, but with a significantly smaller proportion of elastic fibres Conclusions The lesions we examined in these young HIV-1-infected patients presented particular features and were intermediate between the lesions observed during common coronary atherosclerosis and atherosclerosis associated with chronic rejection of cardiac transplants, Coronary Artery Dis 11:41-46 (C) 2000 Lippincott Williams & Wilkins.
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